EricPotratz

Here's somethin' to chew on - 5α-Reductase inhibitors alter steroid metabolism and may contribute to insulin resistance, diabetes, metabolic syndrome and vascular disease: a medical hypothesis.

So far, out of all the natural extracts, including fatty acids, safflower (carthamus tinctorius) appears to be one of the most potent inhibitors of 5a-reductase found in nature, which is associated with increasing both hair growth, and hair follicle number. 5α-reductase inhibition and hair growth promotion of some Thai plants traditionally used for hair treatment Kumar N, Rungseevijitprapa W, Narkkhong NA, Suttajit M, Chaiyasut C J. Ethnopharmacol., 2011

This is an excerpt from my current work. I can give you guys the full references if you want any of them - Vitamin D (i.e., 25-hydroxycholecalciferol, Vitamin D2) deficiency does not appear to be correlated to male pattern baldness, at least for men in Australia. (Bolland et al. 2008) In females, low Vitamin D levels are strongly correlated to pattern baldness and diffuse hair loss, with the most severe forms of hair loss being associated with serum Vitamin D2 <15 nmol/L. (Rasheed et al. 2013) This study also indicated that a serum Vitamin D2 level of about 75 nmol/L may be ideal. (Rasheed et al. 2013) Over 50% of the U.S. adult population has < 60 nmol/L serum Vitamin D2, and thus may benefit from additional vitamin D. (Sciences 2012) Interestingly, it appears that sun exposure is required to express the Vitamin D receptor, which may be more important than vitamin D itself. (Lesiak et al. 2011; Demay 2012) The Vitamin D receptor is required for growth cycling, and is activated not only by Vitamin D, but also fatty acids and various phytochemicals. (Jurutka et al. 2007; Demay 2012; Aoi et al. 2012; Rasheed et al. 2013) Vitamin D is also known as a critical factor in the production of anti-inflammatory T regulatory cells. (Issazadeh-Navikas et al. 2012) Some practitioners feel that Vitamin D supplementation offers no benefit for hair loss sufferers. (Krutmann and Humbert 2010) While this may be true, perhaps moderate sun exposure will offer benefit by increasing production of both Vitamin D, and the critical Vitamin D receptor. (Lesiak et al. 2011)

Yes, good study. I hadn't seen it before. Low androgen levels are generally linked to insulin resistance, so I'm surprised the finasteride didn't show a more negative effect on IR values in that study considering the suppression of DHT.

Not sure if there is a placebo controlled trial on finasteride based around insulin sensitivity but there plenty of evidence to suggest that a dramatic reduction in circulating androgen is going to negatively affect insulin sensitivity. (see post #9 in this thread) Poor insulin sensitivity, means poor blood sugar control, which could bouts of mental fog. (and of course whatever direct GABAergic effects finasteride or its affected hormones may impart)

Nobody is talking about 5a-reductase isoforms. It has no relevance here. Finasteride flatout cuts circulating DHT by 70%. And both insulin sensitivity and cognitive function are negatively influenced from reduced circulating androgen levels. See post #9 for references.

Hairweare, 5a-reductase is not a hormone receptor, its a conversion enzyme. The androgen receptor (AR) is the receptor. The lack of DHT, leads to lack of stimulus on the AR, which leads to lack of glucose uptake and impaired mental function. Doesn't matter where the DHT originally came from. My background is 10 years of male hormone product formulation. You can find more info about me on google.

We are talking about the negative mental effects of reduced circulating DHT, not the location of 5a-reductase. The type of 5a-reductase, or its location, doesn't matter in this situation. FYI, the majority of circulating DHT comes from 5a-reductase action in the prostate.

Yes sir. Finasteride reduces circulating DHT about 70%. (1) Since DHT is about 3-4x more potent than testosterone as an androgen, this equates to about a 50% drop in total androgen bioactivity. (2) Considering the average testosterone level for an adult male is around 500ng/dL, a 50% drop in total bioactivity would equate to roughly 250ng/dL testosterone level, which can be defined as hypogonadism. (3) Hypogonadism leads to decline in mental function, most notably forgetfulness and fogginess. (4,5) I have the full texts of these references if you want them. 1. Finasteride in the treatment of men with androgenetic alopecia. Finasteride Male Pattern Hair Loss Study Group Kaufman KD, Olsen EA, Whiting D, Savin R, DeVillez R, Bergfeld W et al. J. Am. Acad. Dermatol., 1998 2. Serum Androgen Bioactivity During 5a-Dihydrotestosterone Treatment in Elderly Men Raivio T, Tapanainen JS, Kunelius P, Janne OA J. Androl., 2002 3. Prevalence of hypogonadism in males aged at least 45 years: the HIM study Mulligan T, Frick MF, Zuraw QC, Stemhagen A, McWhirter C Int. J. Clin. Pract., 2006 4. The male climacterium: clinical signs and symptoms of a changing endocrine environment van den Beld AW, Lamberts SW Prostate Suppl., 2000 5. Testosterone and cognitive function: current clinical evidence of a relationship. Beauchet O. Eur J Endocrinol. 2006 Dec;155(6):773-81.

Thats an interesting perspective. Unfortunately, inhibiting androgen bioactivity by nearly 50% (finasteride) will result in general loss of insulin sensitivity, which is sufficient to precipitate metabolic disorders (e.g., brain fog).

Finasteride does induce a state of hypogonadism and inhibits insulin sensitivity. This is probably the cause of brain fog, as a result of insulin being less effective at delivering glucose to brain cells. However, I'm not sure if finasteride has direct neuroactive effects, so this might also be a contributor.

Whey protein is not my first choice for hair growth. If you are severely protein deficient whey can help, but its highly insulinemic and causes a big spike in circulating IGF-1 which can increase 5a-reductase levels in the scalp and promote DHT related hair loss. Fresh animal proteins (e.g., grass fed beef, organ meats, mussels, etc) are going to be a superior source of protein with much less effect on IGF-1.